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Ribosomal proteins mediate non-canonical regulation of gut inflammatory signature by crop contaminant deoxynivalenol.
Ecotoxicol Environ Saf
January 2025
Laboratory of Mucosal Exposome and Biomodulation, Department of Integrative Biomedical Sciences, Pusan National University, Yangsan, Republic of Korea; Biomedical Research Institute, Pusan National University, Busan, Republic of Korea; Graduate Program of Genomic Data Sciences, Pusan National University, Yangsan, Republic of Korea; Program of Total Foodtech and PNU-Korea Maritime Institute (KMI) Collaborative Research Center, Busan, Republic of Korea. Electronic address:
Deoxynivalenol (DON), a prevalent mycotoxin produced by Fusarium species, contaminates global agricultural products and poses significant health risks, particularly to the gastrointestinal (GI) system. DON exposure disrupts ribosomal function, inducing stress responses linked to various inflammatory diseases, including inflammatory bowel disease (IBD). In this study, we elucidate a novel regulatory mechanism involving ribosomal proteins (RPs) RPL13A and RPS3, which mediate proinflammatory chemokine production in DON-exposed gut epithelial cells.
View Article and Find Full Text PDFDeath by ribosome.
Trends Cell Biol
December 2024
Center for Gene Expression, Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3B, DK-2200 Copenhagen, Denmark. Electronic address:
Next to their essential role as protein production factories, ribosomes serve as molecular sensors of cell stress. Stalled and collided ribosomes trigger specific stress signaling, including the ribotoxic stress response (RSR). The RSR is initiated by the mitogen-activated protein (MAP)-3 kinase ZAKα in response to a plethora of translational aberrations, leading to activation of the stress-activated MAP kinases p38 and jun N-terminal kinase (JNK).
View Article and Find Full Text PDFThe ribotoxic stress response drives acute inflammation, cell death, and epidermal thickening in UV-irradiated skin in vivo.
Mol Cell
December 2024
Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3, 2200 Copenhagen, Denmark; Center for Gene Expression, Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3, 2200 Copenhagen, Denmark. Electronic address:
Solar UVB light causes damage to the outermost layer of skin. This insult induces rapid local responses, such as dermal inflammation, keratinocyte cell death, and epidermal thickening, all of which have traditionally been associated with DNA damage response signaling. Another stress response that is activated by UVB light is the ribotoxic stress response (RSR), which depends on the ribosome-associated mitogen-activated protein 3 kinases (MAP3K) ZAKα and culminates in p38 and JNK activation.
View Article and Find Full Text PDFRoles of cytochromes P450 and ribosome inhibition in the interaction between two preoccupying mycotoxins, aflatoxin B1 and deoxynivalenol.
Sci Total Environ
December 2024
INRAE, UMR1331, Toxalim, Research Centre in Food Toxicology, Toulouse, France. Electronic address:
Article Synopsis
- * This study focused on the interaction between two significant mycotoxins: aflatoxin B1 (AFB1), a strong carcinogen, and deoxynivalenol (DON), which is commonly found in food.
- * Findings reveal that DON reduces the harmful effects of AFB1 by inhibiting the activity of enzymes that activate AFB1, suggesting the need to study these toxins together rather than in isolation.
Metabolic stress must be effectively mitigated for the survival of cells and organisms. Ribosomes have emerged as signaling hubs that sense metabolic perturbations and coordinate responses that either restore homeostasis or trigger cell death. As yet, the mechanisms governing these cell fate decisions are not well understood.
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